Beta blockade, ventricular arrhythmias, and sudden cardiac death

The mechanisms precipitating sudden cardiac death may be ischemic, electrical, or mechanical. Activation of the autonomic nervous system leads to an increase in sympathetic tone, increasing blood pressure, shear forces, heart rate, platelet aggregation, and blood viscosity while decreasing heart-rate variability and lowering the ventricular fibrillation threshold. Such changes increase the likelihood of plaque rupture or erosion and platelet aggregation, resulting in ischemic or electrical sudden cardiac death. Management of benign ventricular arrhythmias should consist largely of abstinence from sympathetic nervous system stimulants; when pharmacotherapy is required, beta-adrenergic blockers are the agents of choice. Optimal therapy for potentially lethal ventricular arrhythmias is not yet firmly established for amiodarone and implantable cardioverter-defibrillator (ICD) use; however, appropriate secondary prevention utilizes aspirin, beta blockers, angiotensin-converting enzyme inhibitors, and revascularization procedures. Currently, ICDs are established as a first-choice intervention for malignant ventricular arrhythmias, while the adjunctive and independent use of beta-blocker therapy and amiodarone is undergoing further investigation.